CPT1B and post-traumatic stress disorder: Altogether, utilizing a mitochondria-focused gene microarray approach in conjunction with our previous human brain data,4 the results from these three independent experiments (stressed-rat amygdala, stressed-rat blood and PTSD subject blood) support the hypothesis that dysregulation of mitochondria-focused gene(s),2 specifically CPT1B in the fatty acid metabolism and PPAR pathways, may be a part of the pathology of PTSD (Figure 4c).